[Effect of the novel aminoadamantane derivative A-7 on Parkinsonian syndrome induced by systemic administration of neurotoxin MPTP]. / Vliianie novogo proizvodnogo aminoadamantana A-7 na proiavleniia parkinsonicheskogo sindroma, vyzvannogo sistemnym vvedeniem neirotoksina MFTP.

A new antiparkinsonian drug, N-(2-adamantyl)hexamethyleneimine hydrochloride (A-7), was studied on the model of parkinsonism syndrome (PS) induced by MPTP neurotoxin. A-7 (5-20 mg/kg) attenuated the MPTP induced akinesia and rigidity manifestations in C57B1/6 mice, the effect being more pronounced than that of cyclodol and levodopa and comparable to that of midantane (amantadine). A-7 also decreased the PS manifestations in rats: removed tremor, rigidity, and oligokinesia, normalized the MPTP-violated bioelectrical activity of nucleus caudatus, sensomotor cortex, and dorsal hippocamp, and eliminated pathologic slow activity, paroxysmal discharges, and high-frequency activity discharges. The activity of A-7 exceeded that of levodopa (enhancing tremor) and cyclodol (not eliminating the pathologic slow activity).

[The pharmacological properties of karazedin]. / O farmakologicheskikh svoistvakh karazedina.

The original agent 1,2,3,4,5,5a,6,10b-octahydroazepino-[4,5-b]indole (carazedine), an analog of the highly active antipsychotic drug carbidine, was synthesized. This agent was found to have various psychotropic activities and to be superior to carbidine, as shown by a number of tests, and combine properties typical of neuroleptics and tranquilizers. The toxicity of carazedine and carbidine was equal.

[Lipid peroxidation in the caudate nuclei in experimental parkinsonian syndrome]. / Perekisnoe okislenie lipidov v kvostatykh iadrakh pri éksperimental'nom parkinsonicheskom sindrome.

Lipid peroxidation was investigated in adult (8-10 months of age) rat striatum with Parkinsonian syndrome induced by MPTP and its metabolite MPP+. MPTP 20 mg/kg i.p. 4 doses) produced a slight enhancement of lipid peroxidation and significant increase when MPP+ (0.04 mg/kg) was injected into the substantia nigra.

[Reception and extrareceptor binding of cytostatic serotonin antagonists by early embryos of the sea urchin Arbacia lixula]. / Retseptsiia i vneretseptornoe sviazyvanie tsitostaticheskikh antagonistov serotonina rannimi zarodyshami morskogo ezha Arbacia lixula.

Unfertilized eggs and early embryos of the sea urchin Arbacia lixula incubated for 60 min in a medium containing the antagonists of prenervous serotonin, i.e. inmecarb (21 microM) or imipramine (40 microM), bind up to 5 microM of these drugs per 1 ml of cells. At high cell concentrations (more than 10,000 eggs or embryos per 1 ml), this binding is not followed by inhibition of cleavage divisions or by increase in the sensitivity to cytostatic effects of these drugs, which is taken as an indication that this binding is a nonreceptive one. The decrease in concentration of eggs or embryos does not affect total binding of the drugs, although their antiserotonin effects become evident indicating the existence of the receptor sites of binding. In experiments with 3H-imipramine, two binding pools were found (Bmax being correspondingly equal to about 20 and 0.75 microM/ml of embryos; the values of Kd amount to 200 and 15 microM). One of them is a nonreceptive pool, whereas the other presumably coincides with receptor binding sites of prenervous serotonin antagonists.

[Experimental parkinsonian syndrome in rats induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine]. / Eksperimental'nyi parkinsonicheskii sindrom u krys, vyzvannyi 1-metil-4-fenil-1,2,3,6-tetragidropiridinom.

Systemic administration of high doses of MPTP caused transient bradykinesia, "freezing" episodes, head tremors, hunching of the back and peripheral autonomic effects. Neurological syndrome was clearly dose-dependent. It has been established that Parkinson's syndrome is caused by high-amplitude paroxysmal discharges in the nucleus caudatis. It is concluded that the nucleus caudatis plays the role of a pathological determinant structure in the development of Parkinson's syndrome induced by MPTP.